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Transcriptome-wide identification of STING agonist programed B cells

ABSTRACT: We employed RNA-seq to study the transcriptomic change in B lymphocytes in response to STING agonist. Transcriptomic analysis of wild type and TMEM173–/– B cells stimulated with STING agonist revealed that the inflammatory response pathway enriched in 3'3'-cGAMP treated WT B cells but lacking in Tmem173-/-B cells comprised of a cluster containing inhibitory regulators, provoking STING signal to evade immune surveillance by inducing an immunosuppressive B cell population.

ORGANISM(S): Mus musculus

PROVIDER: GSE199343 | GEO | 2022/08/10

REPOSITORIES: GEO

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The transcriptome alteration in tumoral NK cells in response to dual or monotherapy of STING agonist and IL-35 blocking antibodies

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Project description:Activation of the STING (Stimulator of Interferon Genes) pathway by microbial or self-DNA, as well as cyclic di nucleotides (CDN), results in the induction of numerous genes that suppress pathogen replication and facilitate adaptive immunity. However, sustained gene transcription is rigidly prevented to avoid lethal STING-dependent pro-inflammatory disease by mechanisms that remain unknown. We demonstrate here that after autophagy-dependent STING delivery of TBK1 (TANK-binding kinase 1) to endosomal/lysosomal compartments and activation of transcription factors IRF3 (interferon regulatory factors 3) and NF-κB (nuclear factor kappa beta), that STING is subsequently phosphorylated by serine/threonine UNC-51-like kinase (ULK1/ATG1) and IRF3 function is suppressed. ULK1 activation occurred following disassociation from its repressor adenine monophosphate activated protein kinase (AMPK), and was elicited by CDN’S generated by the cGAMP synthase, cGAS. Thus, while CDN’s may initially facilitate STING function, they subsequently trigger negative-feedback control of STING activity, thus preventing the persistent transcription of innate immune genes. Total RNA obtained from primary STING deficient mouse embryonic fibroblast reconstituted with mSTING (W), S365A variant (A), or S365D variant (D). These cells were transfected with dsDNA (ISD) for 3 hours.

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Cholesterol removal improves performance of a model biomimetic system to co-deliver a photothermal agent and a STING agonist for cancer immunotherapy

Project description:Biological membranes often play important functional roles in biomimetic drug delivery systems. We discover that the circulation time and targeting capability of biological membrane-coated nanovehicles can be significantly improved by reducing cholesterol level in the coating membrane. A proof-of-concept system using cholesterol-reduced and PD-1-overexpressed T cell membrane to deliver a photothermal agent and a STING agonist is thus fabricated. Comparing with normal membrane, this engineered membrane increases tumor accumulation by ~2-fold. On melanoma mice model, tumors are eliminated with no recurrence in >80% mice after intravenous injection and laser irradiation; while on colon cancer mice model, ~40% mice are cured without laser irradiation. Data suggest that the engineered membranes escape immune surveillance to avoid blood clearance while keeping functional surface molecules exposed. In summary, we develop a simple, effective, safe and widely-applicable biological membrane modification strategy. This “subtractive” strategy displays unique advantages and is worth further development.

2023-08-02 | PXD044151 | Pride

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